ArticleJournal of cellular and molecular medicine2020
G9α-dependent histone H3K9me3 hypomethylation promotes overexpression of cardiomyogenesis-related genes in foetal mice.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- Epigenetic regulation of cardiovascular diseases induced by behavioral and environmental risk factors: Mechanistic, diagnostic, and therapeutic insights.FASEB bioAdvances · 2024Review
- Corrigendum.Journal of cellular and molecular medicine · 2022Article
- Epigenetics in Congenital Heart Disease.Journal of the American Heart Association · 2022Review
- Review
- Construction and investigation of a circRNA-associated ceRNA regulatory network in Tetralogy of Fallot.BMC cardiovascular disorders · 2021Article
- Interactions between the ERK1/2 signaling pathway and PCAF play a key role in PE‑induced cardiomyocyte hypertrophy.Molecular medicine reports · 2021Article
- G9α-dependent histone H3K9me3 hypomethylation promotes overexpression of cardiomyogenesis-related genes in foetal mice.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
- Erratum issuedCorrigendum.2022
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alcohol consumption during pregnancy can cause foetal alcohol syndrome and congenital heart disease. Nonetheless, the underlying mechanism of alcohol-induced cardiac dysplasia remains unknown. We previously reported that alcohol exposure during pregnancy can cause abnormal expression of cardiomyogenesis-related genes, and histone H3K9me3 hypomethylation was observed in alcohol-treated foetal mouse heart. Hence, an imbalance in histone methylation may be involved in alcohol-induced cardiac dysplasia. In this study, we investigated the involvement of G9α histone methyltransferase in alcohol-induced cardiac dysplasia in vivo and in vitro using heart tissues of foetal mice and primary cardiomyocytes of neonatal mice. Western blotting revealed that alcohol caused histone H3K9me3 hypomethylation by altering G9α histone methyltransferase expression in cardiomyocytes. Moreover, overexpression of cardiomyogenesis-related genes (MEF2C, Cx43, ANP and β-MHC) was observed in alcohol-exposed foetal mouse heart. Additionally, we demonstrated that G9α histone methyltransferase directly interacted with histone H3K9me3 and altered its methylation. Notably, alcohol did not down-regulate H3K9me3 methylation after G9α suppression by short hairpin RNA in primary mouse cardiomyocytes, preventing MEF2C, Cx43, ANP and β-MHC overexpression. These findings suggest that G9α histone methyltransferase-mediated imbalance in histone H3K9me3 methylation plays a critical role in alcohol-induced abnormal expression cardiomyogenesis-related genes during pregnancy. Therefore, G9α histone methyltransferase may be an intervention target for congenital heart disease.
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